No abstract available.
Methylprednisolone*

Drug Stability ; Methylprednisolone Hemisuccinate ; administration & dosage

OBJECTIVE: To observe histological changes of the intervertebral disc injected with intradiscal steroid and mollification of discogenic pain. METHOD: A study group of 25 Sprague-Dawely rats was divided into five subgroups. A control group of 10 Sprague-Dawely rats was divided into five subgroups. The rats' intervertebral discs were exposed by an anterior surgical approach. For study group, the rats were injected intradiscally methylprednisolone acetate 4 mg (Depomedrol, 40 mg/ml) to the L4-L5 intervertebral disc, methylprednisolone sodium succinate 4 mg (Solumedrol, 40 mg/ml) to the L5-L6 intervertebral disc, and triamcinolone acetonide 4 mg (Triamcinolone, 40 mg/ml) to the L6-S1 intervertebral disc. For control group, the rats were injected intradiscally 0.1 ml of saline to the L5-L6 intervertebral disc and a needle was inserted in the L6-S1 intervertebral disc. The intervertebral discs were extracted after 1 week, 2 weeks, 3 weeks, 4 weeks, and 16 weeks. The extracted intervertebral discs were stained with Hematoxylin-Eosin and examined histomorphometrically. RESULTS: There is no significant histological change in either group until 4 weeks after the different types of steroid were injected. Focal fibrotic change was present in the Solumedrol and Triamcinolone injection subgroups after 16 weeks. CONCLUSION: We concluded that rapid mollification of discogenic pain following intradiscal steroid injection may not result from histological change of the disc. Further biochemical study will be neccessary to clarify mollification mechanism of discogenic pain by intradiscal steroid injection.
Animals ; Intervertebral Disc* ; Methylprednisolone ; Methylprednisolone Hemisuccinate ; Needles ; Rats ; Triamcinolone ; Triamcinolone Acetonide

The purpose of this study was to determine the beneficial effect of treatment with methylprednisolone sodium succinate on the cytochrome oxidase activity and lipid peroxidation during 4 hour after 400gm-cm injury to the cat spinal cord. The contusion injury was associated with a decrease of the cytochrome oxidase activity of the gray matter and an increase of the lipid peroxidation. A significant drop in cytochrome oxidase activity to about 40% of normal level was observed as early as 15 minutes after injury and the lowest activity was reached at 1 hour postinjury, but at 4 hours after injury the level of the activities of the enzyme was increased or stabilized. An increase of lipid peroxidation began as early as 15 minutes after the injury and the highest concentration was reached at 4 hour of postinjury. An intravenous dose of 30mg/kg methylprednisolone sodium succinate was administered immediately after the injury. The significant increased of the cytochrome oxidase activity and concomitant decrease of the lipid peroxidation were found in cats of the treated methylprednislone. These results suggest that the beneficial effects of 30mg/kg dose administration of the methylprednisolone are an enhancement of cytochrome oxidase activity, ie., the mitochondria function and an attenuation of lipid peroxide formation, as the result of the inhibition of the O2-free radial reaction.
Animals ; Cats ; Contusions ; Cytochromes* ; Electron Transport Complex IV* ; Lipid Peroxidation* ; Methylprednisolone Hemisuccinate ; Methylprednisolone* ; Mitochondria ; Spinal Cord Injuries ; Spinal Cord*

Recent clinical trials have reported that methylprednisolone sodium succinate administered within 8 hours improves neurological recovery in human spinal cord injury (SCI). Methylprednisolone, however, was ineffective and possibly even deleterious when given more than 8 hours after injury. This finding suggests that a therapeutic time window exists in spinal cord injury. In order to determine the doses, durations and timing of methylprednisolone treatment for optimal neuroprotection, a single or two bolus dose of methylprednisolone (30 mg/kg) was administered at 10, 30, 120, 150 and 240 min. after three graded spinal cord injury. The primary outcome measure was 24-hour spinal cord lesion volumes estimated from spinal cord Na+ and K+ shifts. A single 30 mg/kg dose of methylprednisolone at 10 min. after injury significantly reduced 24-hour lesion volumes in injured rat spinal cords. However, any other methylprednisolone treatment starting 30 min. or more after injury had no effect on 24-hour lesion volumes compared to the vehicle control group. Moreover, delayed treatment increased lesion volumes in some cases. These results suggest that the NYU SCI model has a very short therapeutic window.
Animal ; Drug Administration Schedule ; Male ; Methylprednisolone Hemisuccinate/therapeutic use ; Methylprednisolone Hemisuccinate/administration & dosage* ; Neuroprotective Agents/therapeutic use ; Neuroprotective Agents/administration & dosage* ; Rats ; Rats, Long-Evans ; Spinal Cord/pathology ; Spinal Cord Injuries/pathology ; Spinal Cord Injuries/drug therapy*

This study was performed to investigate the ranges of electrolyte changes during conventional neurosurgical anesthetic management. We selected 20 patients who were operated for brain tumor, intracranial aneurysm and arteriovenous malformation randomly. All patients were received solumedrol preoperatively and managed with hyperventilation (PaCO2: 25-30 torr), solumedrol (1.0 gm), mannitol, furosemide during operation. At 30 and 60 minutes after mannitol infusion, serum electrolytes (Ka+, K+) were checked. The results were as follows: 1) Serum K+ concentration was decreased from 3.96+/-0.46 mEq/L to 3.63+/-0.40 mEq/L in 30 minutes after diuretic administration (p<0.01). 2) At 60 minutes after diuretic administration, serum K+ concentration was decreased from 3.96+/-0.46mEq/L to 3.75+/-0.37mEq/L (p<0.05) and slightly higher than 30 minutes without statistical significance. 3) Serum Na+ concentration was not significantly changed at 30 and 60 minutes after diuretic administration. In conclusion, frequent evaluation of intraoperative serm electrolytes level should be stressed to prevent distortion of it due to hyperventilation and diuretics in neurosurgical anesthetic management.
Arteriovenous Malformations ; Brain Neoplasms ; Brain* ; Diuretics* ; Electrolytes* ; Furosemide ; Humans ; Hyperventilation* ; Intracranial Aneurysm ; Mannitol ; Methylprednisolone Hemisuccinate ; Selective Estrogen Receptor Modulators

Retrobulbar hematoma is a rare condition caused by direct trauma and postopertive complication. But, if prompt treatments delayed, retobular hematoma can cause catastrophic loss of vision. Proposed mechanism of visual loss by retrobulbar hematoma are increased intraocular pressure, retinal ischemia secondary to central artery occlusion, optic nerve compression and resultant ischemia. When retobulbar hematoma is suspected, medical and surgical treatment are needed. Which includes intravenous osmotic agents, acetazolamide, and beta-blocker eyedrops and prompt surgical exploration, such as lateral canthotomy. We report a case of retrobular hematoma occurred in closed reduction on zygoma fracture of 56-years-old female. In operation, abrrupt mydriasis, exophthalmos, and chemosis are detected and eyeball movement restriction observed. so we consulted these situation to ophthalmologist. He examined the patient and diagnosed as retrobulbar hematoma. So we ceased operation and incised lateral canthotomy promptly and solumedrol 500mg, 15% mannitol 500ml injected intravenously. Postoperative 2 days later, periorbital swelling and chemosis still remained, but mydriasis and eyeball movement restriction are disappeared.
Acetazolamide ; Arteries ; Exophthalmos ; Female ; Hematoma* ; Humans ; Intraocular Pressure ; Ischemia ; Mannitol ; Methylprednisolone Hemisuccinate ; Mydriasis ; Ophthalmic Solutions ; Optic Nerve ; Retinaldehyde ; Zygoma*

Objective To evaluate the effect of methylprednisolone sodium succinate combined with tropisetron on postoperative nausea and vomiting(PONV)under microvascular decompression of hemifacial spasm.Methods From January to June 2019,485 patients undergoing microvascular decompression for facial spasm at Department of Neurosurgery,Peking University People's Hospital were randomly assigned into two groups with random number table method.For group A(n=242),2 ml saline was administrated by intravenous drip before induction and 5 mg tropisetron after operation.For group B(n=243),40 mg methylprednisolone sodium succinate was administrated by intravenous drip before induction and 5 mg tropisetron after operation.The anesthesia time,operation time,and incidence of PONV in 0-24 h and 24-48 h were recorded for the comparison of the remedial treatment rate of nausea and vomiting between the two groups.Results There was no significant difference in age,gender,smoking history,body mass index value,American Society of Anesthesiologists score,medical history,surgical side,PONV history,operation time or anesthesia time between the two groups(all P > 0.05).The incidence of PONV in group A was 35.5% and 18.2% during 0-24 h and 24-48 h,respectively,which was significantly higher than that(18.5%,χ
Antiemetics ; Double-Blind Method ; Hemifacial Spasm/surgery* ; Humans ; Indoles ; Methylprednisolone Hemisuccinate/therapeutic use* ; Microvascular Decompression Surgery ; Tropisetron

Systemic corticosteroid arrests the progression of vitiligo and leads to repigmentation, but it may produce side effects. It has been reported that the maximum effect for corticosteroid can be achieved without major side effects when it is used at high doses over a short period of time. Recently, narrowband UVB has been used to treat vitiligo. However, there have been no reports on the effectiveness for a combined treatment with narrowband UVB and systemic corticosteroid. We encountered 2 cases of vitiligo patients who had rapid and effective repigmentation after combination therapy with high dose methylprednisolone and narrowband UVB. Intravenous high dose (25 mg/kg) of methylprednisolone for 3 days was followed by narrowband UVB once or twice weekly. After 2 months, rapid improvements were seen in both patients with >75% repigmentation. Combination treatment with high dose methylprednisolone therapy and narrowband UVB may be an effective therapeutic option for vitiligo.
Humans ; Methylprednisolone ; Vitiligo

No abstract available.
Methylprednisolone* ; Purpura, Thrombocytopenic, Idiopathic*